Conclusion
MiR-143 suppresses lens epithelial cell proliferation, invasion and migration by regulating BRD2, which may support a novel therapeutic strategy for cataract patients.
Methods
Clustering analysis was conducted to systematically compare miRNA expression levels across cataract and myopia. The levels of miR-143 and Bromodomain containing 2 (BRD2) were determined using real-time quantitative PCR (RT-qPCR) assay in lens epithelial cells. Transwell and wound healing assays were conducted to detect cell invasive and migratory abilities. The regulation relationship between MiR-143 and BRD2 was assessed using dual-luciferase reporter gene assays. BRD2 was knocked down using siRNA-BRD2, and siRNA-BRD2, and miR-143 inhibitors were transfected into cells with lipofectamine 2000.
Objective
Cataract causes the greatest number of blindnesses worldwide. This study aims to investigate the role of miR-143 in lens epithelial cells.
Results
Through retrieving five databases, 2690 miRNAs were selected. Volcano plot results demonstrated that 200 miRNAs were differentially expressed between cataract and myopia, in which 152 miRNAs were upregulated and 48 miRNAs downregulated in myopia compared with cataract. MiR-143 was upregulated in cataract compared with myopia (P<0.05). MiR-143 inhibitor suppressed the proliferation, invasion and migration of lens epithelial cells (all P<0.05). Luciferase reporter assays confirmed that BRD2 was a miR-143 target gene in SRA01/04 cells. Knockdown of BRD2 promoted SRA01/04 cell proliferation, invasion and migration (all P<0.05). In addition, silencing of BRD2 partially reversed the functions of miR-143 inhibitor on proliferation, invasion and migration (all P<0.05).